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    Multiple P450s and Variation in Neuronal Genes Underpins the Response to the Insecticide Imidacloprid in a Population of Drosophila melanogaster

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    Author
    Denecke, S; Fusetto, R; Martelli, F; Giang, A; Battlay, P; Fournier-Level, A; O'Hair, RA; Batterham, P
    Date
    2017-09-12
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Batterham, Philip; Fournier-Level, Alexandre; O'Hair, Richard
    Affiliation
    School of Chemistry
    School of BioSciences
    Metadata
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    Document Type
    Journal Article
    Citations
    Denecke, S., Fusetto, R., Martelli, F., Giang, A., Battlay, P., Fournier-Level, A., O'Hair, R. A. & Batterham, P. (2017). Multiple P450s and Variation in Neuronal Genes Underpins the Response to the Insecticide Imidacloprid in a Population of Drosophila melanogaster. SCIENTIFIC REPORTS, 7 (1), https://doi.org/10.1038/s41598-017-11092-5.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257013
    DOI
    10.1038/s41598-017-11092-5
    Abstract
    Insecticide resistance is an economically important example of evolution in response to intense selection pressure. Here, the genetics of resistance to the neonicotinoid insecticide imidacloprid is explored using the Drosophila Genetic Reference Panel, a collection of inbred Drosophila melanogaster genotypes derived from a single population in North Carolina. Imidacloprid resistance varied substantially among genotypes, and more resistant genotypes tended to show increased capacity to metabolize and excrete imidacloprid. Variation in resistance level was then associated with genomic and transcriptomic variation, implicating several candidate genes involved in central nervous system function and the cytochrome P450s Cyp6g1 and Cyp6g2. CRISPR-Cas9 mediated removal of Cyp6g1 suggested that it contributed to imidacloprid resistance only in backgrounds where it was already highly expressed. Cyp6g2, previously implicated in juvenile hormone synthesis via expression in the ring gland, was shown to be expressed in metabolically relevant tissues of resistant genotypes. Cyp6g2 overexpression was shown to both metabolize imidacloprid and confer resistance. These data collectively suggest that imidacloprid resistance is influenced by a variety of previously known and unknown genetic factors.

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